Evidence that C9ORF72 Dipeptide Repeat Proteins Associate with U2 snRNP to Cause Mis-splicing in ALS/FTD Patients-Reference-Cited by-同舟云学术

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Evidence that C9ORF72 Dipeptide Repeat Proteins Associate with U2 snRNP to Cause Mis-splicing in ALS/FTD Patients

Published:2017-06 Issue:11 Volume:19 Page:2244-2256
ISSN:2211-1247
Container-title:Cell Reports
language:en
Short-container-title:Cell Reports

Author:

Yin Shanye,Lopez-Gonzalez Rodrigo,Kunz Ryan C.,Gangopadhyay Jaya,Borufka Carl,Gygi Steven P.,Gao Fen-Biao,Reed Robin

Funder

NIH

ALS Therapy Alliance

ALS Association

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference49 articles.

1. Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons;Almeida;Acta Neuropathol.,2013

2. Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS;Ash;Neuron,2013

3. The SMN complex: an assembly machine for RNPs;Battle;Cold Spring Harb. Symp. Quant. Biol.,2006

4. The C9ORF72 GGGGCC expansion forms RNA G-quadruplex inclusions and sequesters hnRNP H to disrupt splicing in ALS brains;Conlon;eLife,2016

5. Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions;Cooper-Knock;Brain,2014

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1. Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging;Ageing Research Reviews;2024-09

2. Disruption of nuclear speckle integrity dysregulates RNA splicing in C9ORF72-FTD/ALS;Neuron;2024-08

3. The exocyst subunit EXOC2 regulates the toxicity of expanded GGGGCC repeats in C9ORF72-ALS/FTD;Cell Reports;2024-07

4. Reversal of C9orf72 mutation-induced transcriptional dysregulation and pathology in cultured human neurons by allele-specific excision;Proceedings of the National Academy of Sciences;2024-04-15

5. Nuclear pore dysfunction and disease: a complex opportunity;Nucleus;2024-02-21

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